Time course of vasodilatory responses in skeletal muscle arterioles: role in hyperemia at onset of exercise

2000 ◽  
Vol 279 (4) ◽  
pp. H1715-H1723 ◽  
Author(s):  
Stacy A. Wunsch ◽  
Judy Muller-Delp ◽  
Michael D. Delp
Keyword(s):  
Skeletal Muscle ◽  
Time Course ◽  
Muscle Blood Flow ◽  
Dynamic Exercise ◽  
Organ Bath ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Exercise Muscle ◽  
Gastrocnemius Muscles ◽  
Hyperemic Response

At the onset of dynamic exercise, muscle blood flow increases within 1–2 s. It has been postulated that local vasodilatory agents produced by the vascular endothelium or the muscle itself contribute to this response. We hypothesized that only vasodilators that act directly on the vascular smooth muscle could produce vasodilation of skeletal muscle arterioles in <2 s. To test this hypothesis, we determined the time course of the vasodilatory response of isolated skeletal muscle arterioles to direct application of potassium chloride, adenosine, acetylcholine, and sodium nitroprusside. Soleus and gastrocnemius muscles were dissected from the hindlimbs of male Sprague-Dawley rats. First-order arterioles (100–200 μm) were isolated, cannulated on micropipettes, and pressurized to 60 cmH2O in an organ bath. Vasodilatory agents were added directly to the bath, and diameter responses of the arterioles were recorded in real time on a videotape recorder. Frame-by-frame analysis of the diameter responses indicated that none of the vasodilator agents tested produced significant diameter increases in <4 s in either soleus or gastrocnemius muscle arterioles. These results indicate that, although these local vasodilators produce significant vasodilation of skeletal muscle resistance arterioles, these responses are not rapid enough (within 1–2 s) to contribute to the initiation of the exercise hyperemic response at the onset of dynamic exercise.

Blood flow in normal and denervated muscle during exercise in conscious rats

1988 ◽  
Vol 255 (6) ◽  
pp. H1509-H1515 ◽  
Author(s):  
M. D. Delp ◽  
R. B. Armstrong
Keyword(s):  
Blood Flow ◽  
Muscular Activity ◽  
Sprague Dawley ◽  
Blood Flows ◽  
Sprague Dawley Rats ◽  
Mechanical Factors ◽  
Denervated Muscles ◽  
Gastrocnemius Muscles ◽  
Low Intensity Exercise ◽  
Hyperemic Response

The purpose of this study was to test the hypothesis that extrinsic mechanical factors, i.e., the dynamic shortening and lengthening imposed on a muscle during limb movements and the rhythmic compressions as surrounding muscles contract and relax, contribute to the initial muscle hyperemia during locomotion in conscious male Sprague-Dawley rats. Soleus and lateral head of gastrocnemius muscles were surgically denervated in one hindlimb several hours before exercise to remove 1) local metabolic vasodilator effects, 2) vasoconstrictor or vasodilatory influences mediated through sympathetic postganglionic fibers, and 3) intrinsic mechanical pumping. Blood flow was measured with radioactive microspheres during preexercise and at 30 s and 5 min of exercise in rats walking at 15 m/min or a motor-driven treadmill. Glycogen concentrations were also measured as an indicator of muscular activity to verify the denervation. Blood flows to control muscles in the normal limb were similar to previously reported values during preexercise and exercise. Denervation, however, decreased preexercise blood flow (69–88%) to muscle composed predominantly of oxidative fibers and increased flow (53%) to muscle composed predominantly of glycolytic fibers. During exercise, blood flow to denervated muscles either remained unchanged or decreased. These data suggest that extrinsic mechanical factors do not significantly contribute to the initial hyperemic response at the onset of low-intensity exercise in normal muscle.

Vitamin E Concentration in Rat Skeletal Muscle and Liver after Exercise

1998 ◽  
Vol 8 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Jon N. Swift ◽  
James P. Kehrer ◽  
K. Stephen Seiler ◽  
Joseph W. Starnes
Keyword(s):  
Skeletal Muscle ◽  
Vitamin E ◽  
High Performance ◽  
Time Course ◽  
Vastus Lateralis ◽  
Sprague Dawley ◽  
Rat Skeletal Muscle ◽  
Sedentary Control ◽  
Sprague Dawley Rats ◽  
Response To Exercise

The purpose of this study was to determine whether submaximal exercise significantly changes the concentration of vitamin E (αToc) in rat liver and skeletal muscle and to establish a time course for the return to basal levels. Male Sprague-Dawley rats, age 8 to 10 weeks, were randomly divided into sedentary control (Con) (n = 7) and exercise n = 17) groups. Exercised animals ran 100 min on a motorized treadmill at approximately 70% VO2max for 3 consecutive days. They were then sacrificed immediately postexercise (0Post), 24 hr post (24Post), or 72 hr post (72Post). The gastrocnemius, red vastus lateralis (RV), white vastus lateralis (WV), and liver were excised and analyzed for αToc concentration by high-performance liquid chromolography utilizing electrochemical detection. We found that after 3 consecutive days of exercise, αToc was reduced in RV and WV at 0Post and 24Post but returned to control values by 72Post. Liver αToc content was not changed at OPost but was significantly reduced at 24 Post and 72 Post. No significant changes in αToc were observed in the gastrocnemius in response to exercise. The data indicate that following an exercise-related decrease, skeletal muscle vitamin E concentration requires more than 24 hr to return to the preexercise concentration, and that the replenishment process may involve redistribution of vitamin E from liver to muscle.

Effects of arterial hypotension on microvascular oxygen exchange in contracting skeletal muscle

2006 ◽  
Vol 100 (3) ◽  
pp. 1019-1026 ◽  
Author(s):  
Brad J. Behnke ◽  
Danielle J. Padilla ◽  
Leonardo F. Ferreira ◽  
Michael D. Delp ◽  
Timothy I. Musch ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Contractile Function ◽  
Muscle Blood Flow ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Exercise Onset ◽  
Muscle Contractile ◽  
Hypovolemic Hypotension

In healthy animals under normotensive conditions (N), contracting skeletal muscle perfusion is regulated to maintain microvascular O2 pressures (Pmv[Formula: see text]) at levels commensurate with O2 demands. Hypovolemic hypotension (H) impairs muscle contractile function; we tested whether this condition would alter the matching of O2 delivery (Q̇o2) to O2 utilization (V̇o2), as determined by Pmv[Formula: see text] at the onset ofmuscle contractions. Pmv[Formula: see text] in the spinotrapezius muscles of seven female Sprague-Dawley rats (280 ± 6 g) was measured every 2 s across the transition from rest to 1-Hz twitch contractions. Measurements were made under N (mean arterial pressure, 97 ± 4 mmHg) and H (induced by arterial section; mean arterial pressure, 58 ± 3 mmHg, P < 0.05) conditions; Pmv[Formula: see text] profiles were modeled using a multicomponent exponential fitted with independent time delays. Hypotension reduced muscle blood flow at rest (24 ± 8 vs. 6 ± 1 ml−1·min−1·100 g−1 for N and H, respectively; P < 0.05) and during contractions (74 ± 20 vs. 22 ± 4 ml−1·min−1·100 g−1 for N and H, respectively; P < 0.05). H significantly decreased resting Pmv[Formula: see text] and steady-state contracting Pmv[Formula: see text](19.4 ± 2.4 vs. 8.7 ± 1.6 Torr for N and H, respectively, P < 0.05). At the onset of contractions, H reduced the time delay (11.8 ± 1.7 vs. 5.9 ± 0.9 s for N andH, respectively, P < 0.05) before the fall in Pmv[Formula: see text] and accelerated therate of Pmv[Formula: see text] decrease (time constant, 12.6 ± 1.4 vs. 7.3 ± 0.9 s for N and H, respectively, P < 0.05). Muscle V̇o2 was reduced by 71% at rest and 64% with contractions in H vs. N, and O2 extraction during H averaged 78% at rest and 94% during contractions vs. 51 and 78% in N. These results demonstrate that H constrains the increase of skeletal muscle Q̇o2 relative to that of V̇o2 at the onset of contractions,leading to a decreased Pmv[Formula: see text]. According to Fick's law, this scenario will decrease blood-myocyte O2 flux, thereby slowing V̇o2 kinetics and exacerbating the O2 deficit generated at exercise onset.

Contribution of arterial feed vessels to skeletal muscle functional hyperemia

1994 ◽  
Vol 76 (4) ◽  
pp. 1512-1519 ◽  
Author(s):  
J. M. Lash
Keyword(s):  
Skeletal Muscle ◽  
Vascular Resistance ◽  
Muscle Blood Flow ◽  
Aerobic Exercise Training ◽  
Functional Hyperemia ◽  
Sprague Dawley ◽  
Tissue Pressure ◽  
Sprague Dawley Rats ◽  
A Site ◽  
Induced Changes

The purpose of this study was to determine whether dilation of arterial vessels preceding the microcirculation contributes differentially to increases in skeletal muscle blood flow during contractions in anesthetized sedentary (SED) or trained (TR) rats. Experiments were performed in the spinotrapezius muscle of adult male Sprague-Dawley rats. Before and immediately after muscle contractions (2, 4, or 8 Hz), intravascular pressures, red blood cell velocities, and vessel diameters were measured in terminal feed arteries at a site before penetration into the tissue. Pressure was also measured in the accompanying vein. Contraction-induced changes in vascular resistance were calculated for upstream (Rup), spinotrapezius muscle microvascular (Rst), and downstream segments. At rest, Rup accounted for less (32 vs. 40%) and Rst for more (59 vs. 47%) of total resistance in TR than in SED rats. At 8 Hz, contractions produced significantly greater functional dilation (SED, 138 +/- 14 microns; TR, 178 +/- 12 microns) and hyperemia (SED, 11.9 +/- 3.2 x control; TR, 16.8 +/- 3.1 x control) in TR than in SED rats. Inflow pressures did not change, and outflow pressures increased significantly with contractions. Rup and Rst each decreased 60–80% after 2-Hz contractions and > 90% after 8-Hz contractions. Therefore, feed artery dilation contributes significantly to functional hyperemia in the rat spinotrapezius muscle. Furthermore, it appears that aerobic exercise training results in a redistribution of segmental vascular resistance between feed vessels and the microcirculation.

Myogenic and nonmyogenic cells differentially express proteinases, Hsc/Hsp70, and BAG-1 during skeletal muscle regeneration

2003 ◽  
Vol 285 (1) ◽  
pp. E206-E215 ◽  
Author(s):  
Stéphanie Duguez ◽  
Marie-Catherine Le Bihan ◽  
Dominique Gouttefangeas ◽  
Léonard Féasson ◽  
Damien Freyssenet
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Time Course ◽  
Immunohistochemical Analysis ◽  
Inflammatory Cells ◽  
Skeletal Muscle Regeneration ◽  
Nuclear Antigen ◽  
Strongly Correlated ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Skeletal muscle has a remarkable capacity to regenerate after injury. To determine whether changes in the expression of proteinases, 73-kDa constitutive heat shock cognate protein (Hsc70) and stress-inducible 72-kDa heat shock protein (Hsp70) (Hsc/Hsp70), and Bcl-2-associated gene product-1 (BAG-1) contribute to the remodeling response of muscle tissue, tibialis anterior muscles of male Sprague-Dawley rats were injected with 0.75% bupivacaine and removed at 3, 5, 7, 10, 14, 21, or 35 days postinjection ( n = 5–7/group). The immunohistochemical analysis of desmin, α-actin, and developmental/neonatal myosin heavy chain expressions indicated the presence of myoblasts ( days 3–7), inflammatory cells ( days 3–7), degenerating myofibers ( days 3–7), regenerating myofibers ( days 5–10), and growing mature myofibers ( days 10–21) in regenerating muscles. Our biochemical analysis documented profound adaptations in proteolytic metabolism characterized by significant increases in the enzyme activities of matrix metalloproteinases 2 and 9 and plasminogen activators ( days 3–14), calpains 1 and 2 ( days 3–7), cathepsins B and L( days 3–10), and proteasome ( days 3–14). Proteasome activity was strongly correlated with proliferating cell nuclear antigen protein level, suggesting that proteasome played a key role in myoblast proliferation. The expression pattern of BAG-1, a regulatory cofactor of Hsc/Hsp70 at the interface between protein folding and proteasomal proteolysis, did not corroborate the changes in proteasome enzyme activity, suggesting that BAG-1 may promote other functions, such as the folding capacity of Hsc/Hsp70. Altogether, the diversity of functions attributed to proteinases in the present study was strongly supported by the relative changes in the proportion of myogenic and nonmyogenic cells over the time course of regeneration.

Distribution and metabolism of corticotropin-releasing factor in the rat

1986 ◽  
Vol 64 (6) ◽  
pp. 683-688 ◽  
Author(s):  
Bernard Candas ◽  
Josée Lalonde ◽  
Maurice Normand
Keyword(s):  
Time Course ◽  
Corticotropin Releasing Factor ◽  
Metabolic Clearance ◽  
Sprague Dawley ◽  
Rapid Injection ◽  
Sprague Dawley Rats ◽  
Significant Difference ◽  
The Mean ◽  
The Moment ◽  
The One

To develop a mathematical model of the distribution and metabolism of rat corticotropin-releasing factor (rCRF), the time course of 125I-labelled rCRF in plasma was measured in male Sprague–Dawley rats (i) following a rapid injection of 24 ng rCRF/100 g body weight (BW), or (ii) following a rapid injection of 424 ng rCRF/100 g BW, or (iii) during an infusion at a rate ranging from 0.28 to0.73 ng rCRF∙min−1∙100 g BW−1. The comparison of the one-, two-, and three-compartment models shows that the two-pool structure fits better to the dynamics of CRF in plasma as measured in each rat. Following a rapid injection the decay curve occurs in a biphasic manner; the early phase of disappearance is 25 times faster than the late one. There is no significant difference between the estimates of the metabolic clearance rate following both amplitudes of injection (0.40 ± 0.06 and 0.48 ± 0.05 mL∙min−1∙100 g BW−1). The volume of the first pool, 16.8 ± 1.1 mL/100 g BW, is four times larger than the plasma volume. It would thus appear that CRF is rapidly distributed from plasma into several tissues which are represented in the first pool of the model. The mean residence time of every CRF molecule in the second compartment, from the moment of secretion to its elimination, is from three to four times longer than in the first one. It stays, on average, between 140 min and 3 h in the system before an irreversible exit. At steady state, the disposal rate represents only 3% of the CRF mass of the first compartment every minute. These results could explain the prolonged effects of CRF on pituitary-adrenocortical secretion.

Effect of low-potassium diet on rat exercise hyperthermia and heatstroke mortality

1981 ◽  
Vol 51 (1) ◽  
pp. 8-13 ◽  
Author(s):  
R. W. Hubbard ◽  
M. Mager ◽  
W. D. Bowers ◽  
I. Leav ◽  
G. Angoff ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Plasma Potassium ◽  
Heat Illness ◽  
Sprague Dawley ◽  
Heat Gain ◽  
Sprague Dawley Rats ◽  
Low Potassium ◽  
Work Done ◽  
Low K

A total of 182 male Sprague-Dawley rats weighing 250–300 g were fed either a control (n = 122) diet for 32 days. The diets contained either 125 or 8 meq potassium/kg, respectively. Rats fed the low-K diet gained weight at only one-third the rate of controls (1.7 vs. 5.2 g/day), and their skeletal muscle and plasma potassium levels were reduced by 28 and 47%, respectively. When run to exhaustion at either 15 or 20 degrees C, low K+-fed rats accomplished less than one-half of the work done by the controls (26 vs. 53 kg. m) but exhibited a markedly greater rate of heat gain per kilogram-meter of work than controls (0.12 vs. 0.05 degrees C)ambient temperature of 20 degrees C, the rats of the low-K+ group despite large differences in body weight (-25%), run time temperature and twice (33 vs 17%) the mortality rate of the controls. Postexercise increases in circulating potassium (less than 90%) of heat-injured rats raised the plasma levels of low K+-fed rats to normal (5.9 +/- 2.2 meq/l). These results appear to characterize the existence of an insidious and, therefore, undocumented form of fatal exertion-induced heat illness.

Time course of peripheral heterothermy in a homeotherm

1980 ◽  
Vol 239 (1) ◽  
pp. R126-R129 ◽  
Author(s):  
R. T. Brown ◽  
J. G. Baust
Keyword(s):  
Room Temperature ◽  
Time Course ◽  
Temperature Fluctuations ◽  
Temperature Gradients ◽  
Tissue Temperature ◽  
Central Component ◽  
Sprague Dawley ◽  
Contralateral Limb ◽  
Sprague Dawley Rats ◽  
Peripheral Temperature

The integrity of the peripheral heterothermic response was monitored in adult Sprague-Dawley rats during cold acclimation. Subcutaneous peripheral temperature gradients were simultaneously recorded in the hindlimbs. One limb was exposed to room temperature (22 +/- 2 degrees C) while the contralateral limb was gradually cooled to 0 +/- 1 degrees C. Noncontrols were acclimated at 5 +/- 1 degrees C for periods up to 35 days. Controls responded to the cooling regimen (25 to 0 degrees C at 0.5 degrees C . min-1) in a "poikilothermic" manner indicating local cold-induced vasoconstriction (CIVC). CIVC was not released until tissue temperatures reached 22,3 +/- 2.5 degrees C whereupon nonpatterned limb temperature fluctuations, Lewis' hunting response, were often initiated. The hunting response occurred synchronously in the contralateral warmed limb despite its elevated temperature. The experiments revealed a progressive decrease in the intensity of heterothermy indicative of an earlier onset of cold-induced vasodilation as well as increased resistance to tissue cooling with increasing acclimation time. Following 21 days at 5 degrees C, limb exposure to 0 degrees C resulted in a 2-4 degrees C drop in tissue temperature. The time course of the diminution in peripheral heterothermy is discussed. In addition, evidence supporting the hypothesis of a central component in the regulation of the hunting response is presented.

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